Even though the association of endometriosis and infertility is well documented in the literature, very little is known on the mechanisms that ectopic endometrial implants will interfere with normal reproductive function. Different possible mechanisms suggested are: failure of follicular rupture, altered ovum transport, inadequate corpus luteum function and abortion past implantation. We have shown recently that rabbits with induced endometriosis present a low fertility due mainly to a decreased ovulation rate. This impaired reproductive function was associated with increases in prostaglandin F concentrations in peritoneal fluid. The purpose of this study is to examine the mechanisms by which endometriosis may cause infertility. Special emphasis will be applied to the determinations of (1) mechanical factors such as adhesions and/or ovarian endometriosis, (2) incidence of ovulation, (3) incidence of luteal phase defects, and (4) incidence of abortions after implantation. Furthermore, we will attempt to correlate the above mentioned (1-4) factors with (a) concentrations of prostaglandins in peritoneal fluid, (b) local concentrations of prostaglandins in endometriotic implants, and (c) production of prostaglandins by endometriosis (in vitro).